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Anorexia nervosa (AN) is a common eating disorder that affects 2.9 million people worldwide. Not eating a balanced diet or fasting can cause neurological complications after severe vitamin B1 malnourishment, although the precise signs and symptoms of Wernicke's encephalopathy (WE) are not clear. Our aim was to review the signs and symptoms of WE in patients with AN. We searched MEDLINE, EMBASE, Scopus, and PiCarta on all case descriptions of WE following AN. All case descriptions of WE in AN, irrespective of language, were included. Twelve WE cases were reviewed, suggesting that WE following AN is still a relatively rare neuropsychiatric disorder. WE is characterized by a triad of: mental status change, ocular signs, and ataxia. In alcoholism, this triad is present in 16% of cases, but eight out of 12 AN cases presented themselves with a full triad of symptomatology. Importantly, patients often had a more complex triad than has been previously described, involving vertigo, diplopia, and the consequences of refeeding syndrome. The development of a full triad and additional symptomatology suggests a late recognition of signs and symptoms of WE in AN. A complicating factor is the overlap between symptoms of thiamine deficiency and the symptoms of WE. Specifically, patients who show rapid weight loss are vulnerable for the development of WE. Eating disorders, such as AN, can lead to WE. Prophylactic thiamine checks and treatment in patients with AN are relevant, and in case of suspicion of WE, adequate parenteral thiamine supplementation is necessary.

Background: Wernicke-Korsakoff syndrome (WKS) is a neurological disorder typically found in alcohol use disorder. The fact that it also occurs in nonalcoholic patients is less well known and often ignored. For the first time, this review offers a systematic investigation of the frequency and associated features of nonalcoholic WKS in the published literature. Method: We included 11 recent systematic reports, with a total of 586 nonalcoholic WKS cases following hyperemesis gravidarum (n = 177), cancer (n = 129), bariatric surgery (n = 118), hunger strike (n = 41), soft drink diet in children (n = 33), depression (n = 21), Crohn's disease (n = 21), schizophrenia (n = 15), anorexia nervosa (n = 12), ulcerative colitis (n = 10), and incidental thiamine-deficient infant formula (n = 9). Findings: Vomiting and extreme weight loss were strong predictors of nonalcoholic WKS in adults. Blurred vision was a common presenting sign in about one-fourth of the patients. The classic triad of WKS is characterized by confusion, ataxia, and eye-movement disorders. All reviewed studies reported high percentages of patients presenting with an altered mental status, while both motor symptoms were variably present. Interpretation: The foregoing observations led to several important conclusions. First, we can see that nutritional impoverishment leads to profound brain damage in the form of WKS. Second, it seems that physicians are either unaware of or underestimate the risks for nonalcoholic WKS. Physicians must be specifically vigilant in detecting and treating WKS in patients with sudden and severe weight loss and vomiting. Third, lower doses of thiamine frequently lead to chronic Wernicke-Korsakoff syndrome. We noticed that when thiamine treatment for WKS was administered, in many cases doses were too low. In line with proven interventions we therefore recommend a parenteral thiamine treatment of 500 mg 3 times per day in adults.

Introduction: In schizophrenia, patients can experience delusions or hallucinations regarding their food or health status, leading to diminished intake. Fasting or not eating a balanced diet can cause neurological complications after severe vitamin B1 malnourishment. The precise signs and symptoms of Wernicke's Encephalopathy (WE) in schizophrenia are not clear. Our aim, therefore, was to conduct a systematic review of the characteristics of WE in patients with schizophrenia. Methods: We conducted our search from inception using Mesh terms schizophrenia, Wernicke Encephalopathy, Korsakoff's syndrome. We searched Pubmed, ISI Web of Science, and Scopus. We defined WE as mental, oculomotor, and motoric alterations and thiamine deficiency; schizophrenia was defined as psychosis, hallucinations and/or delusions; adequate WE treatment as >500 mg/day intramuscular or intravenous. Our search yielded 15 WE cases. Results: WE is characterised by a triad of mental status change, ocular signs and ataxia. In alcohol use disorder, this triad is present in 16% of the cases, but 12 out of the 15 published schizophrenia cases presented themselves with a full triad. Importantly, as an additional characteristic, patients often lost weight within a short period of time. Conclusions: The development of a full triad and additional symptomatology suggests a late recognition of signs and symptoms of WE in schizophrenia. Prophylactic thiamine checks and treatment in patients with schizophrenia are relevant, and if WE is suspected adequate parenteral thiamine supplementation is necessary. KEY POINTS Only few cases of schizophrenia-related WE have been published in the literature, though challenges in diagnosing and recognising WE suggest that the vast majority of cases go undetected. Acute thiamine deficiency leads to Wernicke's Encephalopathy. Patients diagnosed with schizophrenia are at risk to develop Wernicke's Encephalopathy. Timely treatment with high doses of thiamine can adequately treat Wericke's Encephalopathy.

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Background Korsakoff syndrome (KS) is a severe neuropsychiatric disorder caused by acute deficiency of vitamin B1 and concomitant alcoholism. Patients with KS are particularly vulnerable for cerebrovascular comorbidity. KS is characterized by cognitive and neuropsychiatric symptoms, one of which is apathy. Apathy is a pathological lack of goal‐directed behaviors, goal‐directed cognitions, and goal‐directed emotions. Cerebrovascular accidents are known to carry a risk for developing apathy. Apathy has a dramatic effect on the autonomy and daily lives of patients suffering from this condition. Methods We assessed general apathy and related subconstructs in fifteen patients with KS, fifteen patients with KS and cerebrovascular comorbidity who reside in a 24‐hour care facility, and fifteen healthy controls. Results Compared with healthy controls, both KS patient groups showed higher levels of apathy as rated by a close informant. We found no difference between both KS patient groups and the healthy control group on the self‐report section of the Pleasant Activities List, suggesting that motivation is still intact in KS patients. It is important to note a discrepancy was found between self‐reporting and proxy reporting on this list. KS patients with cerebrovascular comorbidity showed more severe emotional blunting compared to both KS patients without cerebrovascular comorbidity and healthy controls. The competency to consent was lower in patients compared with healthy controls, but no difference was found between KS patients with cerebrovascular comorbidity and those without. Conclusions Our results suggest that KS patients show increased levels of general apathy compared with healthy controls. Patients show a diminished competency to consent and increased emotional blunting, while motivation is not compromised. Cerebrovascular comorbidity in KS forms a high risk for emotional blunting. The results of this study suggest that apathy is a severe problem in KS. More attention in both the literature and clinical practice would benefit this complex patient population.

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